Background
Reversible cerebral vasoconstriction syndrome (RCVS) is a heterogeneous group of cerebrovascular disease that would be presented with thunderclap headache. The pathophysiology of RCVS is unknown, but the prevailing hypothesis involves a disturbance in the control of cerebral vascular tone. Dysregulation of cerebral vascular tone in RCVS may be induced by various hormonal and biochemical factors such as estrogen, serotonin, nitric oxide, prostaglandins, and endothelin-1. Gonadotropin-releasing hormone (GnRH) agonists are a group of drugs that with long-term use induce a pseudomenopausal state in which estrogenproduction are suppressed. It is known that estradiol and estron are all potent enhancers of arterial relaxation and lead to reduction of vascular contraction. The RCVS could be triggered by estrogen withdrawal induced by GnRH agonist. We report a case of RCVS after the injection of synthetic analogue of gonadotropin releasing hormone. 
Case presentation
A 49-year-old woman visited the emergency room with recurrent thunderclap headache. There was no previous history of hypertension and trauma, and there was no other medication except injections. She received a GnRH agonist(Lorelin Depot®) 3.75mg injection subcutaneously because of menorrhagia caused by uterine leiomyoma. She was injected four days before, one month and three months before headache.
Initial evaluation at another hospital, Computed tomography (CT) showed no cerebral hemorrhage. She was discharged home but thunderclap headache and sudden visual field defect occurred the next day, she presented to the emergency room again. CT showed intracerebral hemorrhage(ICH) in the right occipital lobe and subarachnoid hemorrhage in the right Sylvian fissure.
Transfemoral cerebral angiography(TFCA) showed no evidence of aneurysm but there were multifocal narrowings of both middle cerebral arteries. Nifedipine and mannitol was administered but bilateral visual field defect occurred on the fifth day after the onset of right ICH. She was transferred our hospital, CT showed ICH in the left occipital lobe.
Gradient recalled echo image showed the bilateral ICH in the both occipital lobes without evidence of other microbleeding suggesting cerebral amyloid angiopathy. Laboratory analysis revealed that the possibility of inflammatory or rheumatologic, hypercoagulable etiology were ruled out with normal values. Transesophageal echocardiography was performed to rule out septic embolism, there was no intracardiac thrombus. 
The patient received oral dosing of 30 mg of nifedipine three times a day and he was discharged after the headache gradually improved and partial recovery of visual. Until now, there was no recurrence during follow-up.

Discussion
We report a case of RCVS induced by GnRH agonist with a typical clinical and radiological presentation. Synthetic GnRH agonist exerts a maximal effect at 2-4 weeks after subcutaneous injection, and estradiol and estrogen are the lowest concentrations at this time. We didn’t measured the hormone levels directly, but our case showed the close temporal relationship that the patient had a thunderclap headache at the 4th week after the second injection. 
RCVS is predominant in women and is associated with pregnancy. When we consider existing cases, the changes of female hormone levels are likely to be important factors in RCVS. Synthetic GnRH agonist induces a decrease of estrogen. Estrogen is known as a vasodilator which can increase vascular dilation by secreting endothelial-derived vasodilators(e.g NO). Therefore, synthetic GnRH agonist may cause estrogen withdrawal and may cause RCVS due to a decrease in estrogen concentration.

Reversible cerebral vasoconstriction syndrome presenting with bilateral occipital hemorrhage after the subcutaneous injection of synthetic gonadotropin releasing hormone.